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30 Cards in this Set
- Front
- Back
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venous drainage of adrenals
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R- into IVC
L- into renal v |
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adrenal cortex produces
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hormones
-cortisol (glucocorticoid) -aldosterone (mineralcorticoid) -testosterone (androgen) epi & NE & DA |
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histo layers in adrenal
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capsule
zona glomeruluosa (aldost) zona fasiculata (cortisol) zona reticularis (androgens) medulla (epi & NE) |
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production of androgens
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chol to pregnenolone
17 hydoxylase (gives cortisol & DHEA) DHEA to testosterone (21 beta hydroxylase then 11 beta hydroxylase to cortisol) |
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production of cortisol
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chol to pregnenolone (ACTH)
to 11 deoxycortisol (17 hydrox & 21 hydroxylase) to cortisol (11 beta hydroxylase) |
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production of aldosterone
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cholesterol to pregnenolone (AT II)
to progesterone to 11 deoxycorticosterone (beta 21 hydroxylase) to corticosterone (via 11 beta hydroxylase) to aldosterone |
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congenital 17 alpha hydroxylase deficiency
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excessive aldosterone
-HTN & hypokalemia low androgen & low cortisol -phenotypically female but no maturation |
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congenital 21 beta hydroxylase deficiency
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low cortisol
-high ACTH low aldosterone -hypotension, hyponatremia -hyperkalemia -high renin -volume depletion & hypovolemic shock excessive androgen -masculinization -female pseudohermaphroditism |
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congenital 11 beta hydroxylase
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like 21 beta hydroxylase but Hypertension
(11 deoxycorticosterone is weak mineralcorticoid) |
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affects of cortisol
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glucagon acts w/cortisol
activates aldosterone R when excess feedback inhibition of ACTH (suppress insulin, bone growth, immune system increase blood pressure) |
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common glucocorticoids
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hydrocortisone- cortisol
prednisolone & prednisone- -activated by 11 hydroxylase -tx inflammation cortisone -tried for increased performance -no intrinsic activity -liver & kidney activate Dexamethasone -long biol activity on receptor -potent |
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adrenal insufficiency (eg's)
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primary= Addison's
secondary = pituitary tumor tertiary= hypothalamic effect |
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mech of Addison's
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adrenal gland damaged
lose feedback elevated ATCH |
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mech of secondary AI
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pituitary tumor
-adrenal gland atrophy -low ATCH |
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mech of tertiary AI
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hypothalamic defect
-b/c prednisone -pit & HT suppressed -lasts up to a year |
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hyperpigmentation
hypotension fatigue, malaise, anorex Lab: hypoNa, hyperK, acid, low glucose, eos, low Ca, azotemia |
primary AI
Addison's mostly autoimmune -AIDS, ALD, CAH, fungal, TB get elevated ACTH (think JFK) |
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active form glucocorticoid
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cortisol
(activated by 11 beta oxoreductase) (inactivate to cortisone by 11 beta DH) |
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11 beta oxo-reductase
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converts (activates) cortisone to cortisol
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11 beta dehydrogenase
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converts (inactivates cortisol to cortisone)
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normal mineralcorticoid
low glucocort & androgen ACTH stim test Insulin Tolerance test Metyrapone test |
secondary AI
decreased ACTH stim test many false neg give emperical GC rplct if hypotensive |
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first line lab test for AI
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NOT random cortisol
cosyntropin -primary AI <10 -may be low in secondary b/c atrophy |
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f/u lab tests for AI
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ITT
Metyrapone distinguish primary v. secondary via plasma ACTH |
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meaning of negative cosyntropin
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chronic AI excluded
f/u w/ITT, ACTH & metyrapone may be mild or secondary AI |
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features of adrenal crisis
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(acute AI)
mimic sepsis hypoten, CV collapse fever, weak, apathy, confusion dehydrat, hypoNa, hyperK N, V, anorexia hypoglycemia |
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diagnosis of acute AI
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random cortisol
cosyntropin (if stable) treat (if unstable or pos cosyntropin) tx w/IV cortisol |
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high basal cortisol
high free cortisol blunted response to cosyntropin |
relative AI
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examples of hyperaldosteronism
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Cushings
Pheochromocytoma Primary Hyperaldosteronism |
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HTN
weight gain moon facies truncal obesity buffalo hump hyperglycemia (thin skin, osteoporosis, amenorrhea, immune suppression) |
Cushings Syndrome = hypercortisolism
caused by: -Cushing's dz -primary adrenal -ectopic ACTH production -chronic steroids |
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positive dexamethasone supression test
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to test Cushing's
normal: -low cortisol after low dose ACTH producing tumor: -high cortisol after low dose -low cortisol after high dose (normal rspns) Cortisone producing tumor -high cortisol after low or high dose |
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hyperaldosteronism
types & cause |
primary= Conn's syndrome
-aldost secreting tumor -has LOW plasma renin secondary -renal artery stenosis, renal failure, CHF, cirrhosis or nephrotic syndrome -has HIGH plasma renin |
